title: Frequency of CCR5-Delta32 deletion in human immunodeficiency virus type 1 (HIV-1) in healthy blood donors, HIV-1-exposed seronegative and HIV-1-seropositive individuals of southern Brazilian population.
abstract: The frequency of CCR5-Delta32 allele in human immunodeficiency virus type 1 (HIV-1) infection in the southern Brazilian population was determined in a cross-sectional study carried out from October 2001 to June 2004. Genomic DNA was extracted from peripheral blood cells of 134 healthy blood donors, 145 HIV-1-exposed seronegative individuals, 152 HIV-1-seropositive asymptomatic individuals, and 478 HIV-1-seropositive individuals with AIDS. A fragment with 225 base-pairs of the CCR5 gene was amplified by polymerase chain reaction. The CCR5-Delta32 homozygous deletion was observed in 2 (1.5%) blood donors and in 1 (0.7%) individual HIV-1-exposed seronegative, and was absent among all the HIV-1-seropositive individuals (Fisher's exact test, p=0.0242). The frequency of the homozygous CCR5-Delta32 deletion in the HIV-1-exposed did not differ when compared with that observed in the HIV-1 seronegative blood donors (Fisher's exact test, p=0.6093; OR: 2.18, 95% CI: 0.11-129.6). The wild-type genotype CCR5/CCR5 frequency was higher among the HIV-1-seropositive with AIDS compared to HIV-1 seropositive asymptomatic individuals (Chi-square test, p=0.0263; OR: 2.02, 95% CI: 1.03-3.97). The absence of the homozygous deletion of CCR5-Delta32 among HIV-1-seropositive individuals underscored that this genotype is an important genetic factor associated with the decreased susceptibility to HIV-1 infection. The higher frequency of heterozygosity for the CCR5-Delta32 and the CCR5-Delta32 allele in HIV-1 seropositive asymptomatic compared to HIV-seropositive with AIDS individuals also underscored that this deletion could be associated with the delay of the HIV-1 disease progression in this population. However, the low frequency of CCR5-Delta32 homozygosity observed among HIV-1-exposed seronegative individuals shows that the allele could not explain, by itself, the natural resistance to HIV-1 infection and different mechanisms of protection against HIV-1 infection that must be involved in this population.
authors.affiliation: Health Sciences Center, Department of Pathology, Clinical Analysis and Toxicology, University Hospital of Londrina State University, Vila Operária, CEP 86.038-440, Londrina, Paraná, Brazil. reiche@sercomtel.com.br
authors.forename: Edna Maria Vissoci
authors.initials: EM
authors.lastname: Reiche
authors.forename: Maria Angelica
authors.initials: MA
authors.lastname: Ehara Watanabe
authors.forename: Ana Maria
authors.initials: AM
authors.lastname: Bonametti
authors.forename: Helena Kaminami
authors.initials: HK
authors.lastname: Morimoto
authors.forename: Arilson
authors.initials: A
authors.lastname: Akira Morimoto
authors.forename: Susana Lílian
authors.initials: SL
authors.lastname: Wiechmann
authors.forename: Tiemi
authors.initials: T
authors.lastname: Matsuo
authors.forename: Jaqueline
authors.initials: J
authors.lastname: Carvalho De Oliveira
authors.forename: Fernando
authors.initials: F
authors.lastname: Vissoci Reiche
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000235:genetics* / Q000276:immunology; D000483:Alleles; D001782:Blood Donors; D001938:Brazil; D005260:Female; D005787:Gene Frequency / Q000235:genetics / Q000276:immunology; D018023:HIV Seronegativity / Q000235:genetics*; D006679:HIV Seropositivity / Q000235:genetics* / Q000276:immunology; D015497:HIV-1 / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics*; D008297:Male; D019713:Receptors, CCR5 / Q000235:genetics* / Q000276:immunology; D017384:Sequence Deletion
chemical_list: D019713:Receptors, CCR5